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自身免疫性甲状腺炎中的IP - 10

IP-10 in autoimmune thyroiditis.

作者信息

Ruffilli I, Ferrari S M, Colaci M, Ferri C, Fallahi P, Antonelli A

机构信息

Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

Department of Medical, Surgical, Maternal, Pediatric and Adult Sciences, University of Modena and Reggio Emilia, Modena, Italy.

出版信息

Horm Metab Res. 2014 Aug;46(9):597-602. doi: 10.1055/s-0034-1382053. Epub 2014 Jun 30.

DOI:10.1055/s-0034-1382053
PMID:24977661
Abstract

The interferon-γ-inducible protein 10 (IP-10) was initially identified as a chemokine that is induced by interferon (IFN)-γ. IP-10 exerts its function through binding to chemokine (C-X-C motif) receptor 3 (CXCR3). IP-10 and its receptor, CXCR3, appear to contribute to the pathogenesis of many autoimmune diseases, organ specific (such as type 1 diabetes, Graves' disease and ophthalmopathy), or systemic (such as systemic lupus erythematosus, mixed cryoglobulinemia, Sjogren syndrome, or systemic sclerosis). The secretion of IP-10 by (CD)4+, CD8+, and natural killer is dependent on IFN-γ. Under the influence of IFN-γ, IP-10 is secreted by thyrocytes. Determination of high level of IP-10 in peripheral fluids is therefore a marker of a T helper 1 orientated immune response. High levels of circulating IP-10, have been shown in patients with autoimmune thyroiditis (AT). Among patients with AT, IP-10 levels were significantly higher in those with a hypoechoic ultrasonographic pattern, which is a sign of a more severe lympho-monocytic infiltration, and in those with hypothyroidism. For these reasons, it has been postulated that IP-10 could be a marker of a stronger and more aggressive inflammatory response in the thyroid, subsequently leading to thyroid destruction and hypothyroidism. Further studies are needed to investigate whether IP-10 is a novel therapeutic target in AT.

摘要

γ干扰素诱导蛋白10(IP-10)最初被鉴定为一种由γ干扰素(IFN-γ)诱导产生的趋化因子。IP-10通过与趋化因子(C-X-C基序)受体3(CXCR3)结合发挥其功能。IP-10及其受体CXCR3似乎在许多自身免疫性疾病的发病机制中起作用,这些疾病包括器官特异性疾病(如1型糖尿病、格雷夫斯病和眼病)或全身性疾病(如系统性红斑狼疮、混合性冷球蛋白血症、干燥综合征或系统性硬化症)。(CD)4+、CD8+和自然杀伤细胞分泌IP-10依赖于IFN-γ。在IFN-γ的影响下,甲状腺细胞分泌IP-10。因此,外周液中高水平的IP-10是T辅助细胞1型定向免疫反应的一个标志物。自身免疫性甲状腺炎(AT)患者循环中IP-10水平较高。在AT患者中,超声检查呈低回声模式(这是更严重的淋巴细胞浸润的迹象)的患者以及甲状腺功能减退患者的IP-10水平显著更高。基于这些原因,有人推测IP-10可能是甲状腺中更强且更具侵袭性的炎症反应的标志物,随后导致甲状腺破坏和甲状腺功能减退。需要进一步研究以调查IP-10是否是AT的一个新的治疗靶点。

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